Pregnancy is associated with an enormous increase in uterine perfusion, which results from increased maternal cardiac output and trophoblast-driven modification of the uterine spiral arteries. Failure of this normal physiological process is implicated in the aetiology of two of the most challenging obstetric complications, pre-eclampsia (PET) and fetal growth restriction (FGR), also called intra-uterine growth retardation (IUGR).
FGR affects up to 8% of all pregnancies, and is associated with a high perinatal mortality rate, long-term neurological impairment and an increased incidence of cardiovascular disease in later life; there is no effective evidence-based treatment. Severe early onset FGR affects 1:500 pregnancies, and is associated with high mortality and long term complications in survivors. An affected fetus may never achieve a viable delivery weight (at least 500 g) and the parents face a stark choice between termination of pregnancy, or allowing the fetus to die in utero. Small improvements in fetal growth (e.g. to a birthweight of 700 g) and in gestation at birth (e.g. from 26 to 28 weeks) are associated with major improvements in survival and morbidity.
Current antenatal care is designed to detect women who have growth restricted fetuses. A number of strategies such as maternal serum markers and uterine artery Doppler ultrasound examination are available, which may be able to predict the likelihood of the woman developing these conditions. However, there are currently no therapeutic strategies that will successfully prevent the development of FGR.